Inflammatory cytokines and carpal tunnel syndrome: A causal relationship revealed

IF 3.7 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cytokine Pub Date : 2024-10-11 DOI:10.1016/j.cyto.2024.156777

Chen-fei Yang , Ying Pu , Li Li , Ming-gang Guo , Zhi-wei Feng

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引用次数: 0

Abstract

Objectives

Carpal tunnel syndrome (CTS) and certain inflammatory cytokines have been linked in observational studies; however, the exact causative linkages remain unknown. The purpose of this study is to investigate any possible link between the onset of CTS and 91 inflammatory cytokines.

Methods

A two-sample bidirectional Mendelian randomization (MR) approach was used in this investigation. 91 circulating inflammatory cytokines’ genetic variants were retrieved from the European ancestry genome-wide association study (GWAS) database. From germline GWAS, summary data for 24,766 CTS patients and 360,538 controls were gathered. The instrumental variables were single nucleotide polymorphisms (SNPs) that were highly correlated with the 91 inflammatory cytokines. The random-effects inverse-variance weighted (IVW) approach was employed in the primary analysis, and multiple comparisons were subjected to the Bonferroni correction. Sensitivity analysis was performed to evaluate the validity of the causal relationship.

Results

Our findings showed a negative correlation between CCL19, FGF-19, IL-5, TGF-alpha, TRAIL, and the risk of CTS. Specifically, CCL19 (odds ratio [OR]: 0.944, 95 % confidence interval [CI]: 0.894–0.996, p = 0.0349), FGF-19 (OR: 0.940, 95 % CI: 0.894–0.987, p = 0.0133), IL-5 (OR: 0.936, 95 % CI: 0.885–0.990, p = 0.0212), TGF-alpha (OR: 0.902, 95 % CI: 0.838–0.970, p = 0.0057), and TRAIL (OR: 0.926, 95 % CI: 0.881–0.974, p = 0.0026) were inversely related to CTS risk. Conversely, CCL20, IL-2RB, and IL-6 were positively associated with an increased risk of CTS. Specifically, CCL20 (OR: 1.072, 95 % CI: 1.005–1.142, p = 0.0334), IL-2RB (OR: 1.067, 95 % CI: 1.001–1.137, p = 0.0463), and IL-6 (OR: 1.088, 95 % CI: 1.005–1.177, p = 0.0365) were positively correlated with CTS risk. Reverse Mendelian randomization analyses indicated no evidence of a reverse causal relationship between CTS and inflammatory cytokines.

Conclusion

According to this study, there is a causal link between CTS and certain inflammatory cytokines, which suggests that these cytokines may be important in the pathophysiology of CTS. To confirm these results and investigate the specific function of these cytokines in the beginning and development of CTS, more investigation is necessary.

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炎性细胞因子与腕管综合征：揭示因果关系

目的在观察性研究中，腕管综合征（CTS）与某些炎症细胞因子有关联；但确切的因果关系仍不清楚。本研究旨在调查 CTS 发病与 91 种炎症细胞因子之间可能存在的联系。从欧洲血统全基因组关联研究（GWAS）数据库中提取了 91 种循环炎性细胞因子的遗传变异。从种系全基因组关联研究中收集了 24,766 名 CTS 患者和 360,538 名对照组的汇总数据。工具变量是与 91 种炎症细胞因子高度相关的单核苷酸多态性（SNPs）。主要分析采用随机效应逆方差加权（IVW）方法，多重比较采用 Bonferroni 校正。我们的研究结果表明，CCL19、FGF-19、IL-5、TGF-α、TRAIL 与罹患 CTS 的风险呈负相关。具体而言，CCL19（几率比 [OR]：0.944，95% 置信区间 [CI]：0.894-0.996，p = 0.0349）、FGF-19（OR：0.940，95 % CI：0.894-0.987，p = 0.0133）、IL-5（OR：0.936，95 % CI：0.885-0.990，p = 0.0212）、TGF-α（OR：0.902，95 % CI：0.838-0.970，p = 0.0057）和 TRAIL（OR：0.926，95 % CI：0.881-0.974，p = 0.0026）与 CTS 风险成反比。相反，CCL20、IL-2RB 和 IL-6 与 CTS 风险增加呈正相关。具体来说，CCL20（OR：1.072，95 % CI：1.005-1.142，p = 0.0334）、IL-2RB（OR：1.067，95 % CI：1.001-1.137，p = 0.0463）和 IL-6（OR：1.088，95 % CI：1.005-1.177，p = 0.0365）与 CTS 风险呈正相关。反向孟德尔随机分析表明，没有证据表明 CTS 与炎性细胞因子之间存在反向因果关系。要证实这些结果并研究这些细胞因子在 CTS 的起始和发展过程中的具体功能，还需要进行更多的研究。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cytokine 医学-免疫学

CiteScore

7.60

自引率

2.60%

发文量

262

审稿时长

48 days

期刊介绍： The journal Cytokine has an open access mirror journal Cytokine: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review. * Devoted exclusively to the study of the molecular biology, genetics, biochemistry, immunology, genome-wide association studies, pathobiology, diagnostic and clinical applications of all known interleukins, hematopoietic factors, growth factors, cytotoxins, interferons, new cytokines, and chemokines, Cytokine provides comprehensive coverage of cytokines and their mechanisms of actions, 12 times a year by publishing original high quality refereed scientific papers from prominent investigators in both the academic and industrial sectors. We will publish 3 major types of manuscripts: 1) Original manuscripts describing research results. 2) Basic and clinical reviews describing cytokine actions and regulation. 3) Short commentaries/perspectives on recently published aspects of cytokines, pathogenesis and clinical results.